DNA methylation as a triage tool for cervical cancer screening – A meeting report

Burdier, F. Ricardo; Waheed, Dur-e-Nayab; Nedjai, Belinda; Steenbergen, Renske D.M.; Poljak, Mario; Baay, Marc; Vorsters, Alex; Van Keer, Severien

doi:10.1016/j.pmedr.2024.102678

Cited by 7 publications

(1 citation statement)

References 55 publications

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“…Genotypes 16 and 18 are the most oncogenic, with HPV 16 alone being responsible for more than 50% of cervical cancers, and both causing 70% of all cervical cancers [8]. Due to the treatment of precancerous lesions, the implementation of screening with HPV testing, colposcopy, and HPV vaccine, it is hoped that cervical cancer can be defeated by 2030 [9][10][11][12][13][14]. The World Health Organization has set a global goal of eliminating cervical cancer, defined as achieving an incidence of fewer than 4 cases per 100,000 women per year [15,16].…”

Section: Introductionmentioning

confidence: 99%

Extended Genotyping to Stratify the Risk of CIN2+ in Women with Persistent HPV Infection, Negative Cytology and Type 3 Transformation Zone

Bruno,

Valenti,

Cavallaro

et al. 2024

Cancers

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Persistent human papillomavirus (HPV) infection is recognized as a major risk factor for cervical cancer. Women with persistent HPV and negative cytology are at greater risk of CIN2+ than women with negative infection. The diagnosis becomes more complicated when the woman has a type 3 transformation zone at colposcopy. The aim of this study was to determine the prevalence of CIN2+ in women with persistent HPV, negative cytology and TZ3; how to stratify the risk of CIN2+; and what the best diagnostic strategy is, given TZ3. Methods: In a multicenter retrospective cohort study, we enrolled women with negative cytology and TZ3 among the 213 women referred for colposcopy for persistent HPV. The average age of the women was 53 years; in particular, 83% were postmenopausal women. In the presence of a TZ3, the entire transformation zone cannot be explored, making colposcopy and targeted biopsy useless and inadequate, with great risks of underdiagnosis or missed diagnosis. Women with TZ3 underwent diagnostic LEEP to ensure correct diagnoses. Results: The study highlighted 19% (16/84) of CIN2+ lesions, a higher frequency of non-HPV 16/18 genotypes (76.2%), and 50% of CIN2+ lesions being due to non-HPV 16/18 genotypes. Furthermore, more than half of the women (80.9%) had normal histopathological results in the LEEP sample. Conclusion. Women with viral persistence, negative cytology, and TZ3 have a 19% risk of CIN2+; genotyping helps stratify risk, but extensive genotyping is necessary instead of partial genotyping (16/18), referring to a population of women over 50 years old in which the prevalence of genotypes 16,18 decreases and the prevalence of other genotypes increases; diagnostic LEEP is excessive (only 16 cases of CIN2+ out of 48 cases treated), even though 83% of women had viral clearance after LEEP; p16/Ki67 double staining could be a potential risk marker, which would only highlight women at risk of CIN2+ to undergo LEEP. To individualize the diagnostic workup and treatment and minimize the risk of under diagnosis and overtreatment, future studies should explore the use of extended genotyping and new biomarkers for individual risk stratification.

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Section: Introductionmentioning

confidence: 99%

Extended Genotyping to Stratify the Risk of CIN2+ in Women with Persistent HPV Infection, Negative Cytology and Type 3 Transformation Zone

Bruno,

Valenti,

Cavallaro

et al. 2024

Cancers

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Will methylation assays be part of a full molecular strategy to improve clinical management of cervical neoplasia?

El-Zein,

Franco

2024

Epigenomics

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Estimating HPV16 genome copy number per infected cell in cervical smears

Elie,

Boué,

Paget-Bailly

et al. 2024

Preprint

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Human papillomavirus (HPV) 16 is the most oncogenic biological agents for humans. However, essential quantitative aspects of its infection cycle remain inadequately characterized. Specifically, the proportion of infected cells and the viral copy number per infected cell in cervical smears are not well understood. To address this, we employed a combination of limiting dilution techniques and Bayesian statistics on routine cervical smears to estimate the frequency of infected cells and the viral copy number per cell. Our methodology was initially validated through numerical simulations and cell culture experiments. Subsequently, we analyzed 38 HPV16-positive cervical smears, comprising 26 samples from patients without cytological lesions and 12 from patients with low-grade lesions. Our findings indicated that the substantial variability in viral load across samples predominantly stemmed from differences in the frequency of infected cells. Additionally, the mean number of HPV copies per infected cell was consistently low across all samples, ranging from approximately 2.3 to 100 copies. However, in samples with low-grade lesionMarie-Paule Algross, this number was observed to double on average. These results challenge existing assumptions regarding the biology of HPV genital infections, which are typically asymptomatic or minimally symptomatic.

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DNA methylation as a triage tool for cervical cancer screening – A meeting report

Cited by 7 publications

References 55 publications

Extended Genotyping to Stratify the Risk of CIN2+ in Women with Persistent HPV Infection, Negative Cytology and Type 3 Transformation Zone

Extended Genotyping to Stratify the Risk of CIN2+ in Women with Persistent HPV Infection, Negative Cytology and Type 3 Transformation Zone

Will methylation assays be part of a full molecular strategy to improve clinical management of cervical neoplasia?

Estimating HPV16 genome copy number per infected cell in cervical smears

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